Several studies have reported that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can directly infect endothelial cells, and endothelial dysfunction is often found in severe cases of coronavirus disease 2019 (COVID-19). To better understand the prognostic values of endothelial dysfunction in COVID-19-associated coagulopathy, we conducted a systematic review and meta-analysis to assess biomarkers of endothelial cells in patients with COVID-19.
A literature search was conducted on online databases for observational studies evaluating biomarkers of endothelial dysfunction and composite poor outcomes in COVID-19 patients.
A total of 1187 patients from 17 studies were included in this analysis. The estimated pooled means for von Willebrand Factor (VWF) antigen levels in COVID-19 patients was higher compared to healthy control (306.42 [95% confidence interval (CI) 291.37-321.48], p?&lt;?0.001; I86%), with the highest VWF antigen levels was found in deceased COVID-19 patients (448.57 [95% CI 407.20-489.93], p?&lt;?0.001; I0%). Meta-analysis showed that higher plasma levels of VWF antigen, tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 antigen (PAI-1) antigen, and soluble thrombomodulin (sTM) were associated with composite poor outcome in COVID-19 patients ([standardized mean difference (SMD) 0.74 [0.33-1.16], p?&lt;?0.001; I80.4%], [SMD 0.55 [0.19-0.92], p?=?0.003; I6.4%], [SMD 0.33 [0.04-0.62], p?=?0.025; I7.9%], and [SMD 0.55 [0.10-0.99], p?=?0.015; I23.6%], respectively).
The estimated pooled means show increased levels of VWF antigen in COVID-19 patients. Several biomarkers of endothelial dysfunction, including VFW antigen, t-PA, PAI-1, and sTM, are significantly associated with increased composite poor outcomes in patients with COVID-19.
CRD42021228821.
CRD42021228821.Management of idiopathic intracranial hypertension (IIH) is recommended after surgical repair of spontaneous cerebrospinal fluid leaks (sCSF-leaks) of the skull base for prevention of recurrence.
To assess the feasibility of venous sinus stenting, a treatment commonly used for the treatment of IIH associated with intracranial venous sinus stenosis (VSS), after sCSF-leaks closure.
A single-center cohort series of consecutive patients who underwent sCSF-leak closure was retrospectively analyzed. https://www.selleckchem.com/Proteasome.html Stenting was considered either for leak recurrence or in prophylactic manner after repair in patients with VSS as confirmed by cerebral venous imaging. Leak recurrence, need for new repair or adjunctive treatment of IIH, meningitis, and stenting complications were determined at the last follow-up. Cases who had prophylactic stenting were compared to historical controls before stenting option.
Twenty-two patients had intracranial venous stenting after sCSF-leak closure. Their median age was 58 years (Q1=45; Q3=68), BMI=31kg.m(Q1=27; Q3=36), and female rate=85%. The overall rate of successful repair after stenting was 95% (95% CI=87-100%) at a median follow-up of 2.4 years (Q1=1.2; Q3=3.3). Adjunctive treatment for IIH was needed in 4 patients (4/22, 18%) including 2 patients without leak recurrence. No meningitis, permanent morbidity or mortality was observed after stenting. Compared to 18 controls, cases had significantly less recurrence (P=0.03), and a trend for less adjunctive treatment for IIH (P=0.06).
Our study suggests that stenting might be a valid option for prevention of sCSF-leak recurrences after repair in patients with intracranial venous sinus stenosis.
Our study suggests that stenting might be a valid option for prevention of sCSF-leak recurrences after repair in patients with intracranial venous sinus stenosis.To utilize a Luminex platform to examine multiple cytokines simultaneously as well as clinical laboratory testing in order to identify markers that predict acute pancreatitis (AP) severity in the pediatric population on admission.
Patients (&lt;19 years) prospectively enrolled over a 4-year period in a single institution AP database were included in separate derivation and validation cohorts. Plasma samples were obtained within 48 hours of admission and stored for analysis. Samples from mild AP and SAP (moderately severe and severe combined) were analyzed using Luminex panels and C-Reactive Protein (CRP) testing.
The derivation cohort examined 62 cytokines in 66 subject samples (20 control, 36 mild AP, 10 SAP) and identified interleukin 6 (IL-6) [P = .02] and monocyte chemotactic protein-1 (MCP-1) [p=0.02] as cytokines that were differentially expressed between mild and SAP. Our validation cohort analyzed 76 cytokines between 10 controls, 19 mild AP and 6 SAP subjects. IL-6 (p=0.02) and MCP-1 (p=0.007) were again found to differentiate mild AP from SAP. CRP values were obtained from 53 of the subjects, revealing a strong association between elevated CRP values and progression to severe disease (P&lt;0.0001).
This study identified and validated IL-6 and MCP-1 as predictors of SAP using 2 distinct cohorts, and showed that CRP elevation is a marker of progression to SAP. These biomarkers have not been extensively studied in the pediatric AP population. Our data allows for risk-stratification of AP patients, and represent novel insight into the immunologic response in SAP.
This study identified and validated IL-6 and MCP-1 as predictors of SAP using 2 distinct cohorts, and showed that CRP elevation is a marker of progression to SAP. These biomarkers have not been extensively studied in the pediatric AP population. Our data allows for risk-stratification of AP patients, and represent novel insight into the immunologic response in SAP.Infectious bacterial and viral diseases that cause hemolysis are considered life-threatening to grass carp (Ctenopharyngodon idellus), which is a species used in aquaculture worldwide. After heme and hemeproteins (Hb) are released as a result of hemolysis, the effect of excess Hb and heme on tissues remains to be characterized. To decipher the mechanisms, after incubation with Hb, we showed that lipopolysaccharide (LPS), Hb, and heme increased the cytotoxicity and secretion of inflammatory cytokines such as interleukin (IL)-6, chemokine (C-C motif) ligand 1 (CCL1), tumor necrosis factor (TNF)-α, IL-6, and IL-1β in vitro, which was due to stimulation of the expression of innate immune receptors, such as nucleotide-binding oligomerization domain (NOD2), toll-like receptor 2 (TLR2), TLR 4, and TLR3. The formation of reactive oxygen species (ROS) and the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-κB were important for increasing the cytokine production to induce heme, Hb, and LPS.